It has been postulated that lipoprotein (a) [Lp(a)] may be the most atherogenic lipoprotein in man. Current laboratory methods for Lp(a) employ immunoquantitation [apo(a)]. Because these methods are hampered by cross-reactivity to plasminogen, apo(a) isoform dependence, antibody heterogeneity, and lack of standardization, none of them is FDA-approved. One third of Lp(a)'s mass is cholesterol, and only one tenth is apo (a). We propose develop a quantitive affinity-chromatographic, and a semiquantitative teststrip methods for Lp(a) cholesterol [Lp(a)-C]. The chromatographic method exploits Lp(a)'s unique high content of carbohydrate, e.g. N-acetyl-glucosamine and sialic acid. Lp(a) from serum is separated from other lipoproteins by binding of its carbohydrate structures to a specific solid-supported lectin. The bound Lp(a) is eluted and analyzed by a highly sensitive enzymic cholesterol reagent. The method enables quantitation of Lp(a)-C on clinical analyzers, together with the traditional lipid profile of cholesterol, triglyceride, HDL-C and LDL-C. In the noninstrumented visual teststrip method, blood from a fingerstick is separated into its cellular and plasma components by an integrated separating member. The plasma is transferred into a lectin- or antibody- impregnated Lp(a) recipient member. The bound lp(a) is washed free of other lipoproteins and assayed in situ for Lp(a). PROPOSED COMMERCIAL APPLICATION: Lp(a) is an independent risk factor for atherosclerotic/thrombotic vascular disease. Strong associations of elevated plasma levels have been demonstrated for coronary heart and cerebrovascular disease. In the U.S. about three quarters of a million people die each year from these disorders. The annual socioeconomic toll of heart disease has been estimated at $60 billion. The U.S. reagent market for lipid and lipoprotein testing in excess of $150 million. Laboratory billings are about $1.5 billion. Not a single laboratory method currently exists for the quantitation of the cholesterol component of Lp(a), a potential major contributor to Lp(a) atherogenicity.